Medical Forum / Diseases and Disorders / AIDS / October 2005
Ok Iconclaster you claim HEPATITIS C is like HIV a nonexistent figment of the imagination
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Gary Stein - 21 Sep 2005 23:44 GMT Then where are the following 29 articles wrong please anaylize them one at a time and post your evidence as to why a particular article is mistaken in it's premises about Hep C.
NATAP - http://www.natap.org
29 RECENT HEPATITIS C ARTICLES posted to NATAP website: http://www.natap.org
1. New Hep C Protease Inhibitor - (09/21/05) http://www.natap.org/2005/HCV/092105_01.htm
2. Liver Injury and Changes in Hepatitis C Virus (HCV) RNA Load Associated with Protease Inhibitor-Based Antiretroviral Therapy for Treatment-Naive HCV-HIV-Coinfected Patients: Lopinavir-Ritonavir versus Nelfinavir - (09/21/05) http://www.natap.org/2005/HCV/092105_02.htm
3. PEGINTERFERON a-2b THERAPY IN ACUTE HEPATITIS C: IMPACT OF ONSET AND DURATION OF THERAPY ON SUSTAINED VIROLOGIC RESPONSE - (09/20/05) http://www.natap.org/2005/HCV/092005_01.htm
4. Fatigue & Hypermetabolism in HCV: high HCV RNA may cause fatigue & interferon appears to reduce fatigue - (09/19/05) http://www.natap.org/2005/HCV/091905_03.htm
5. HCV natural history in the west & developing world: The retrospective and prospective in perspective - (09/19/05) http://www.natap.org/2005/HCV/091905_02.htm
6. (Marijuana/Hash) Endocannabinoids and liver disease - review - (09/19/05) http://www.natap.org/2005/HCV/091905_01.htm
7. Impact of Hepatitis C Virus on Immune Restoration in HIV-Infected Patients Who Start Highly Active Antiretroviral Therapy: A Meta-analysis - (09/14/05) http://www.natap.org/2005/HCV/091405_10.htm
8. Hepatitis C Virus Infection in HIV Type 1-Infected Individuals Does Not Accelerate a Decrease in the CD4+ Cell Count but Does Increase the Likelihood of AIDS-Defining Events - (09/14/05) http://www.natap.org/2005/HCV/091405_09.htm
9. VA Study: HCV Increases Risk of Death Among HAART-Treated HIV+ Patients by 30-80% - (09/14/05) http://www.natap.org/2005/HCV/091405_08.htm
10. Influence of Hepatitis C Virus Infection on HIV-1 Disease Progression and Response to Highly Active Antiretroviral Therapy - (09/14/05) http://www.natap.org/2005/HCV/091405_07.htm
11. Hepatic steatosis with stavudine in HIV/hepatitis C virus co-infection - (09/14/05) http://www.natap.org/2005/HCV/091405_06.htm
12. Promising Therapy for Human Hepatoma (liver cancer, HCC): Telomerase Inhibition by GRN163 - (09/13/05) http://www.natap.org/2005/HCV/091405_05.htm
13. Single (B or C), dual (BC or BD) and triple (BCD) viral hepatitis in HIV-infected patients in Madrid, Spain - (09/13/05) http://www.natap.org/2005/HCV/091405_04.htm
14. Is Cirrhosis Inevitable in HCV? - (09/13/05) http://www.natap.org/2005/HCV/091405_03.htm
15. Insulin resistance is a cause of steatosis and fibrosis progression in chronic hepatitis C - (09/13/05) http://www.natap.org/2005/HCV/091405_01.htm
16. Hepatocellular carcinoma in 40 HIV/HCV-coinfected versus 50 HCV-monoinfected patients. North American HCC in HIV Study Gro (09/09/05) http://www.natap.org/2005/ias/ias_53.htm
17. Caucasians Had Better HCV Viral Load Reductions Than African-Americans During First 3 Days & During Weeks 1-4 After Starting Peg/RBV (09/09/05) http://www.natap.org/2005/ias/ias_52.htm
18. Hepatitis C infection is not associated with systemic HIV-associated non-Hodgkin's lymphoma: a cohort study (09/09/05) http://www.natap.org/2005/ias/ias_51.htm
19. PI & NNRTI Drug Levels in Coinfected Patients (09/09/05) http://www.natap.org/2005/ias/ias_50.htm
20. Pegasys/RBV Improves Histology in Non-Responders & Cirrhotics (09/09/05) http://www.natap.org/2005/ias/ias_49.htm
21. PegIFN/RBV May Be Less Effective in Acute HCV for HIV+ (09/09/05) http://www.natap.org/2005/ias/ias_48.htm
22. PK of Once Daily Regimen: Fosamprenavir/r, Tenofovir and FTC in Naives (09/09/05) http://www.natap.org/2005/ias/ias_47.htm
23. Occult HCV- HCV RNA Found in Liver of Patients Negative for Antibody-HCV & Serum HCV RNA - (09/05/05) http://www.natap.org/2005/HCV/090505_20.htm
24. EDITORIAL COMMENTARY Hepatitis C Virus (HCV) Occult Infection or Occult HCV RNA Detection? - (09/05/05) http://www.natap.org/2005/HCV/090505_10.htm
25. HCV Did Not Persist in Patients with SVR - (09/05/05) http://www.natap.org/2005/HCV/090505_19.htm
26. Divining the role of liver biopsy in hepatitis C - (09/05/05) http://www.natap.org/2005/HCV/090505_18.htm
27. Chronic hepatitis C and 'normal' ALT levels: Treat the disease not the test - (09/05/05) http://www.natap.org/2005/HCV/090505_17.htm
28. Gilead, Achillion initiate phase I trial evaluating GS 9132 for treatment of hep C - (09/05/05) http://www.natap.org/2005/HCV/090505_16.htm
29. Isatoribine, an agonist of TLR7, reduces plasma virus concentration in chronic hepatitis C infection - (09/05/05) http://www.natap.org/2005/HCV/090505_15.htm
If that's not enough for you there are 420 more articels posted at the following URL; http://www.natap.org/hcv.htm
Gary Stein
DavidT - 22 Sep 2005 13:40 GMT You forget, Gary. There is a massive global biomedicalconspiracy that has infiltrated every single academic institute, every hospital and every research laboratory. All employees are co-conspirators paid directly or indirctly by BigPharma to create non-existent organisms and diseases. Of course you will see thousands of studies on Hepatits C - but none of them were really carried out, and all are fraudulent.
Iconoclaster - 25 Sep 2005 01:55 GMT Paper #5 is very exciting. To marketing people, that is, not to scientists:
>"It is estimated that 170 million persons worldwide are chronically infected with HCV, most of whom reside in developing nations and many of whom may be coinfected with HIV and/or HBV and have very limited access to treatment. Even if only 10% of such individuals advanced to cirrhosis, the global burden of this infection is staggering. Thus HCV, like HIV, is a disease of two worlds, one where new infections are rare and effective treatments are available and one where high population density, inadequate preventive strategies and inaccessible treatments maintain HCV as a common disease with devastating consequences."
Now if you read that, doesn't it give you an idea that there's money to be made? This "natural history of HCV" nowhere mentions when or where 'HCV' was discovered or isolated. It just enters the story unobtrusively. Suddenly, it's there. I agree with one point: HCV is like HIV.
Gary Stein - 25 Sep 2005 03:25 GMT 5 sets of personal opinions completely devoid of any discussion of facts don't an argument make Herr Doctor Iconclaster....
Gary Stein
> Paper #5 is very exciting. To marketing people, that is, not to > scientists: [quoted text clipped - 15 lines] > Suddenly, it's there. > I agree with one point: HCV is like HIV. Iconoclaster - 25 Sep 2005 23:39 GMT >"5 sets of personal opinions completely devoid of any discussion of facts don't an argument make Herr Doctor Iconclaster....
Mr. Stein, do you really mean to say that this paper makes any kind of argument? The point we're discussing is the non-existance of HCV, remember?
Iconoclaster - 27 Sep 2005 02:47 GMT Paper #14 Is Cirrhosis Inevitable in HCV?
>"Remember, HIV can accelerate HCV progression up to 5 times more quickly than in HCV monoinfection. It is generally accepted, as also reported from this study, that HCV progresses slowly so if you live long enough cirhhosis will develop. Therefore, HIV/HCV coinfection becomes a more deadly disease. Many more coinfected patients appear to be at risk for developing cirrhosis within a much shorter time than moninfected."
Oh sure! I can believe that. If you're deemed to be infected with HIV, you get treated with HAART. If you had liver trouble already, no matter what caused it, HAART will finish you off.
>"......infection with HCV for over 60 years causes cirrhosis in 71% of infected individuals. Because relationship between the severity of fibrosis and age in Asian patients is similar to that seen in Caucasian patients it is likely that similar rates of cirrhosis will be seen in other patients who are infected for more than 60 years...."
Hey! This paper is fun! If you live long enough, you'll die of something...
And now a word from our sponsor:
>"In summary, if the data gathered in the study are indeed a true reflection of the long-term impact of chronic HCV infection among Asian patients, and if the findings can be extended to other populations, this would clearly indicate that substantially more, perhaps most, persons infected with HCV are likely to reach end-stage liver disease than had been thought hitherto. It also implies that treatment should indeed be universal for all HCV-infected persons, regardless of their histologic status, in the hope of blunting this progression. In addition, it raises the issue of the need for even more transplantation services to accommodate the anticipated (on the basis of this study) "epidemic" of cirrhosis-related end-stage liver disease and cancer that awaits these patients."
I guess the drug therapy and liver transplantation business will be booming in the next 60 years.
So does HCV exist? Who cares...
DavidT - 22 Sep 2005 13:41 GMT You forget, Gary. There is a massive global biomedicalconspiracy that has infiltrated every single academic institute, every hospital and every research laboratory. All employees are co-conspirators paid directly or indirctly by BigPharma to create non-existent organisms and diseases. Of course you will see thousands of studies on Hepatits C - but none of them were really carried out, and all are fraudulent.
montygram - 22 Sep 2005 22:46 GMT No conpiracy required. There is little incentive to question existing dogma, even if it was not properly established in the first place (using controlled, double-blinded experiments, for example).
There are many scientific models that coexist, yet one must be correct, or at least more accurate, than the other. Those who don't examine the points made by the Perth Group, for example, are not doing science, which requires that all scientific challenges be taken seriously. A hypothesis is supposed to be scrutinized; otherwise, we would still believe in a flat earth.
As an example of a what is going on all the time (though the public is not aware of it), the following report is from TODAY. There are similar examples all over the place. Go to www.gilbertling.org and read about how he has tried to get funding for more experiments to clarify his A-I hypothesis, but because a bureaucrat does not like him, the experiments are not getting done.
Wake up and smell the coffee, people!
9/24/2005 "Sugar Helps Control Cell Division"
"...The dogma for decades has been that the cycle of cell division is controlled by the appearance and disappearance of certain proteins called cyclins, but experiments have shown that you can knock out any of these and still get perfectly normal cell division..."
Source: www.sciencedaly.com
The other intesting thing is that there really is no "HIV/AIDS hypothesis," because it varies from one period of time to another and from one place to another. Let's start with exactly what the hypothesis is, otherwise, there can be no scientific debate. Most people in the USA (including doctors) think that after infection, a person will live several years, perhaps a decade or so, then die of "immune system failure," yet there is the following:
"Less than a quarter of HIV-positive men with haemophilia in the United Kingdom are still alive 20-25 years after infection with HIV," So over 20% of people who are already very ill people can live over 25 years or so with HIV.
And then: "... liver disease has become the major cause of death amongst HIV-positive men with haemophilia."
This is not an "AIDS defining illness," nor has anyone suggested it is.
How is this possible? What is the hypothesis, exactly?
Source: Sabin C et al. Twenty five years of HIV in haemophilic men in Britain: an observational study. BMJ, September 16th, 2005 (online edition).
I have accepted my version of the Duesberg challenge, but nobody wants to take me up on it, so they don't even believe in their own nonsense.
Then I asked, hypothetically, if someone did take me up on the challenge, what would you inject me with? I will only allow "pure virus" and an inert susbstance in which to suspend the virus. How are you going to obtain this virus, since it was never isolated? How will you isolate it, exactly? Explain it. Only fragments, either of the wrong size and right shape (according to the dogma, anyway) or of the correct size and wrong shape, have ever been found, and they are most likely from humans cells that destroyed in the massive oxidative stress that actually does cause most of what is called "AIDS" these days (in the USA, at least).
No conspiracy, just stupidity, fear of reprisals and loss of grants, greed, etc. - all the things that make us human.
So take me up on the Duesberg challenge, or we could agreee upon a Hep C challenge. How, exactly, are you going to isolate this "Hep C virus?" If you beleive in a virus, isolate it and let's talk about doing a experiment that will determine who is correct. The problem, of course, is that you cannot isolate what is not present.
Even true believers have to admit the nonsense, though they do it in a quiet way:
"...the virus has not been grown in tissue culture. Thus, basic studies of the virus are not possible and studies are limited to gene sequencing and clinical studies. and clinical studies..."
Source: http://www.hepnet.com/hkn/c11.html
Do you people understand the implications of this? Why can't they grow it? There is no reason, except that it does not exist!
They say: " The virus for hepatitis C was cloned in 1989," but what does this mean, exactly? Again, fragments were found that most likely were part of human cells that underwent tremendous stress and died off. These fragments were cloned and said to be "Hep C." Why? So that a big company could make big money. Does that surprise you? Is it the first example in human history of a company claiming something that is not likely true in order to make huge profits? Do you think everyone in the company understand exactly what is going on at the molecular level? Let's be real now! You are the ones with the naive view of humanity.
The "studies" that allegedly support the virus claim are circular logic - they assume a virus. In science, you cannot assume what you seek to demonstrate. That is what religious debate is often like, for example, assuming the Bible is the word of God, when there is no way to know that scientifically. So of course the studies will appear to support the virus idea. Do they compare this claim to an oxidative stress hypothesis? Find me a citation that answers that question.
I have confidence that I could "cure" "Hep C" in an animal model, but these clowns admit that they have not been able to create one for "Hep C," which is a damning statement by itself. In people, we are dealing with "patients" who have done tremendous damage to themselve, and who usually don't listen to any authorities, let alone those who have no power to enforce their demands (such as doctors), which is why I offer myself up to demonstrate that this is all nonsense. However, because there is no virus, there is no way for anyone to take me up on my offer, even if they were naive enough to do so.
GMCarter - 22 Sep 2005 23:30 GMT >No conpiracy required. There is little incentive to question existing >dogma, even if it was not properly established in the first place >(using controlled, double-blinded experiments, for example). Hey, aren't you the guy that says no one should EVER even sniff an omega-3 fatty acid?
David Canzi -- non-mailable - 23 Sep 2005 03:33 GMT >Most >people in the USA (including doctors) think that after infection, a >person will live several years, perhaps a decade or so, then die of >"immune system failure," The expectation for *U*N*T*R*E*A*T*E*D* people with HIV infection is that about half develop AIDS within a decade.
>yet there is the following: > >"Less than a quarter of HIV-positive men with haemophilia in the United >Kingdom are still alive 20-25 years after infection with HIV," >So over 20% of people who are already very ill people can live over 25 >years or so with HIV. These people are being treated.
 Signature David Canzi "I am not denying anything." -- Celia Farber
Lorenzo+ - 23 Sep 2005 14:22 GMT > The expectation for *U*N*T*R*E*A*T*E*D* people with HIV infection is > that about half develop AIDS within a decade. Nobody remembers... conspiracies are more interesting!
Iconoclaster - 23 Sep 2005 00:44 GMT Thank you, Mr. Stein, for presenting these 29 articles on Hep-C. Hey! That's neat: One for every indicator disease of AIDS! What a coincidence! Of course, I'll need a little time to study them, in order to find out what's wrong with them. There's no doubt, of course, that there IS something worng with them, because Hep-C Virus doesn;'t exist. There is no record of it being isolated. Some hepatic disease agency in this country informed me that there are 9 classes of HCV and more than 100 subclasses. But they gave me absoluely zero information on the physical properties of this 'virus' Not even one puny subclass. Of course they need this many different forms of the virus, because they have to explain away all the different discrepancies of the virus model, and one single virus type couldn't possibly do that. There is another theory that explains all the deaths from liver disease very well: Hepatic damage from all the toxic drugs that are being used to fight that other non-existing virus: HIV. HCV is the "Alibi Virus", so to speak. But don't go away; I'll be back when I've read those papers.
Iconoclaster - 24 Sep 2005 19:57 GMT Oh puhlease!! Here comes Paper #1:
>"These Phase 1 studies investigate SCH 503034 from Schering Plough both as monotherapy and in combination with PEG-Intron in genotype 1 patients who were nonresponders to peginterferon + ribavirin combination therapy. It is important to note that these Phase 1 studies were conducted with a capsule formulation that is viable for larger-scale clinical studies and, potentially, for commercial development."
It says nothing about Hep-C, the virus. It just ASSUMES that's the problem. Schering Plough is plotting a new poison, to be used on hapless patients who have already been half-killed by peginterferon+ribavirin. Ribavirin is a terrible toxin. It's main side effect is hemolytic anemia (= forced apaoptosis of red blood cells) Brrrrr!
Iconoclaster - 25 Sep 2005 01:10 GMT Tadaaaaa! Her comes paper #2:
>"All patients also received open-label lamivudine (150 mg twice daily (3TC, Epivir) and stavudine (40 mg twice daily [d4T, Zerit]; patients weighing <60 kg received 30 mg). All subjects were screened for HCV by means of an HCV ELISA. Seventy (11%) of 653 subjects enrolled in the parent clinical trial were HCV-antibody reactive upon HCV ELISA testing. ".....this analysis confirms that HCV loads increase after HAART initiation and that this increase is associated with appropriate immune reconstitution. These increases may be accompanied by flares in the ALT level."
<Sob!> The same old sh.t as with 'HIV' ! Testing with ELISA, this time with proteins ASSUMED to come from 'HCV'. Also Viral Load testing while at the same time murdering the patient with lamivudine and stavudine.
Any evidence of Hep-C Virus? I'm not seeing it.
GMCarter - 25 Sep 2005 12:33 GMT snip
><Sob!> The same old sh.t as with 'HIV' ! Testing with ELISA, this time >with proteins ASSUMED to come from 'HCV'. Also Viral Load testing while >at the same time murdering the patient with lamivudine and stavudine. > >Any evidence of Hep-C Virus? I'm not seeing it. You haven't looked for it and wouldn't know what to do if the evidence was staring you in the face. At best, you live in a world of technology that has not gotten passed about 1938.
NOTHING in ANY of your posts suggests that your unsujpported opinion should be given more attention than a rat's fart.
George M. Carter
Iconoclaster - 25 Sep 2005 23:43 GMT >"NOTHING in ANY of your posts suggests that your unsujpported opinion should be given more attention than a rat's fart."
Not by you, Mr. Carter. But surely by people who are able to think for themselves. You only have to read this paper to seen that it presents absolutely no evidence in favor of the existance of HCV.
GMCarter - 26 Sep 2005 14:37 GMT >>"NOTHING in ANY of your posts suggests that your unsujpported opinion >should be given more attention than a rat's fart." > >Not by you, Mr. Carter. But surely by people who are able to think for >themselves. You only have to read this paper to seen that it presents >absolutely no evidence in favor of the existance of HCV. So says you based on nothing but your ill-considered opinion.
Iconoclaster - 25 Sep 2005 01:24 GMT Paper #3 is about monotherapy with Peginterferon a-2b:
>"Results: Five untreated subjects had spontaneous recovery and another 4 subjects scheduled to start treatment at weeks 12 or 20 resolved spontaneously before therapy. 79 subjects with persistent viremia were randomized to 3 groups (Table). The end of treatment response was 94% and the overall SVR was 82%. The SVR was better for genotype 4 compared to genotype 1. Earlier treatment (week 8 or 12) was associated with higher SVR particularly in genotype 1. Twelve week therapy was sufficient for genotype 4 while higher SVR rates in genotype 1 patients were achieved with 24 wks treatment (86%). Peginterferon c~-2b monotherapy was well tolerated and associated with significant improvement in the quality of life."
These genotypes depend on what kind of genetic sludge has been used to prime the PCR. Peginterferon a-2b is well-tolerated. As a monotherapy it will not kill you as easily as in combination with Ribavirin. I can believe that. But just waiting until the condition clears up by itself, as happened to 9 subjects, works too.
Iconoclaster - 25 Sep 2005 01:45 GMT Paper #4:
>"Background/Aims: Hypermetabolism is considered to be of clinical interest in liver disease and in several chronic viral infections. Whether resting energy expenditure (REE) increases during chronic hepatitis C is not known. Our aims were: (a) to determine the metabolic state of patients with chronic hepatitis C, and (b) to evaluate the effects of interferon therapy on REE.
Well, this study came out the same way it always happens in the clinic: Some patients respond to treatment, other patients don't.
But wait: The authors claim that the REE is really caused by the virus (HCV):
>"As increased REE was correlated with the virus load but not with histological status or ALT activity, hypermetabolism might be a direct result of HCV replication rather than the consequence of hepatic inflammation."
Yeah, it might... Now if we could only prove that there IS a virus... Hm! Viral load, eh? Isn't that based on quantitative PCR? What did kary Mullis have to say about that?
Iconoclaster - 26 Sep 2005 00:07 GMT Paper #6: (Marijuana/Hash) Endocannabinoids and liver disease - review -
Well, this paper is exactly what the title says it is. But... NOT A WORD ON HCV, or any virus at all. It does contain the following stement:
>"These results suggest that chronic marijuana use, alone or in combination with alcohol or other drugs, may have hepatotoxic effects"
Ouch! That will take away the chance for hippies and other babyboomers to blame all the mysery on some real or imagined virus.
GMCarter - 26 Sep 2005 14:33 GMT >Paper #6: (Marijuana/Hash) Endocannabinoids and liver disease - review - > [quoted text clipped - 7 lines] >Ouch! That will take away the chance for hippies and other babyboomers to >blame all the mysery on some real or imagined virus. Ah...alcohol impairs liver function depending on the dose and duration of use. The hepatotoxicity of marijuana is hardly confirmed by this study; the evidence for it is weak at best.
Alcohol and marijuana do not cause AIDS. Alcohol may of course cause cirrhosis. You think it's just the same as HCV-related cirrhosis, histopathologically speaking?
George M. Carter
Iconoclaster - 27 Sep 2005 01:22 GMT >"Alcohol and marijuana do not cause AIDS. Alcohol may of course cause cirrhosis. You think it's just the same as HCV-related cirrhosis, histopathologically speaking?"
No, for two reasons: 1. Cirrhosis i not the same as hepatitis 2. HCV-related cirrhosis or HCV-anything does not exist. There are many ways to screw up your liver, but a non-existent virus is not one of them. Most kinds of liver damage are caused by toxic chemicals.
Iconoclaster - 26 Sep 2005 00:30 GMT Paper #7: Impact of Hepatitis C Virus on Immune Restoration in HIV-Infected Patients Who Start Highly Active Antiretroviral Therapy: A Meta-analysis -
This is indeed a Meta-analysis, i.e., a literature search and comparison of a number of papers on the subject. The authors note:
>"This meta-analysis is dependent on the published literature, and the studies reviewed are very different in their design. In all of the studies, the increase in the CD4 cell count was a secondary outcome, and many of the studies are statistically underpowered to examine the specific question of interest to us."
Nevertheless, the conclusion of this study is:
>"This meta-analysis shows that patients with HIV-HCV coinfection do, in fact, have less immune reconstitution, as determined by CD4 cell count after 48 weeks of HAART, than do patients with HCV infection alone. "
The auhors don't come up with an explanation of this phenomenon. My objection is that, again, "HCV infection" is taken for granted. Like "HIV infection" it is based on an antibody test. As there is no standard in the form of a pure HCV preparation (if there were, they would have cited a reference), the term "HCV infection" has no real meaning.
Iconoclaster - 26 Sep 2005 00:42 GMT Paper #8: Hepatitis C Virus Infection in HIV Type 1-Infected Individuals Does Not Accelerate a Decrease in the CD4+ Cell Count but Does Increase the Likelihood of AIDS-Defining Events
Well, the title says it all, now doesn't it? If you've tested HIV+, you croak sooner if your liver is screwed up too, and CD4+ cells have nothing to do with that. The paper states:
>"In conclusion, there was an increased number of adverse events in coinfected individuals, compared with individuals infected with HIV-1 alone."
Note that these patients were treated with HAART. Their CD4+ cells went up, but they died anyway of liver disease. This is a very clear example where they sorely need another fantasy virus (HCV) to explain this outcome!
GMCarter - 26 Sep 2005 14:39 GMT >Note that these patients were treated with HAART. Their CD4+ cells went >up, but they died anyway of liver disease. This is a very clear example >where they sorely need another fantasy virus (HCV) to explain this >outcome! So it is your belief that all antiretrovirals used to treat HIV are hepatotoxic.
Iconoclaster - 27 Sep 2005 01:25 GMT >"So it is your belief that all antiretrovirals used to treat HIV are hepatotoxic."
Not necessarily. But Proteinase Inhibitors are.
GMCarter - 27 Sep 2005 12:11 GMT >>"So it is your belief that all antiretrovirals used to treat HIV are >hepatotoxic." > >Not necessarily. But Proteinase Inhibitors are. Really. All of them. "Proteinase"?
Wow. You're arrogance and hubris are stunning in the breadth and scope of absolutely nothing they have to back them.
You give W a run for his money.
George M. Carter
Iconoclaster - 28 Sep 2005 01:36 GMT >"Really. All of them. "Proteinase"? Yes, Mr. Carter. All Protease Inhibitors (excuse the misspelling. It was late at night.
And by the way, It's not a 'run for the moey'. I'm having a field trip, or a field day, or whatever. And you, Mr. Carter... are grasping at straws.
GMCarter - 28 Sep 2005 11:46 GMT >>"Really. All of them. "Proteinase"? > >Yes, Mr. Carter. All Protease Inhibitors (excuse the misspelling. It was >late at night. Why? You're supposed to be the educated expert, aren't you?
I forgive you nothing.
Iconoclaster - 29 Sep 2005 01:13 GMT >"Why? You're supposed to be the educated expert, aren't you? I forgive you nothing."
They didn't have Protease Inhibitors in 1938. They did have good science, though.
GMCarter - 29 Sep 2005 12:18 GMT >>"Why? You're supposed to be the educated expert, aren't you? I forgive >you nothing." > >They didn't have Protease Inhibitors in 1938. They did have good science, >though. And nothing has changed in 67 years in science? remarkable.
Iconoclaster - 29 Sep 2005 22:52 GMT >"And nothing has changed in 67 years in science? remarkable." But a lot has changed in science, Mr. Carter! Mainly the scientists. They were not so corrupt back then. And science was not big-money business then either.
GMCarter - 30 Sep 2005 13:08 GMT >>"And nothing has changed in 67 years in science? remarkable." > >But a lot has changed in science, Mr. Carter! You bet. Pity you didn't bother to keep up with ANY of it.
Gary Stein - 03 Oct 2005 19:24 GMT > >"And nothing has changed in 67 years in science? remarkable." > > But a lot has changed in science, Mr. Carter! Mainly the scientists. > They were not so corrupt back then. And science was not big-money > business then either. Oh please science has always been about money or power or both. Most progress in science can be attributed to war and conflict. Progress in Medicine is of course extremely linked to warfare. The idea that it is otherwise is the result of rationalization on the part of scientists for the most part.
Gary Stein
pauleewhiting - 03 Oct 2005 22:13 GMT "Oh please science has always been about money or power or both. Most progress in science can be attributed to war and conflict. Progress in Medicine is of course extremely linked to warfare. The idea that it is otherwise is the result of rationalization on the part of scientists for the most part."
And let me guess, Gary, you think that this history of science being "about money or power or both" somehow *doesn't* apply to the HIV theory of AIDS, right?
And that the "idea that it is otherwise is the result of rationalization on the part of scientists" *doesn't* apply to the AIDS scientists, right?
Gary Stein - 04 Oct 2005 20:09 GMT > "Oh please science has always been about money or power or both. Most > progress in science can be attributed to war and conflict. Progress in [quoted text clipped - 8 lines] > And that the "idea that it is otherwise is the result of rationalization > on the part of scientists" *doesn't* apply to the AIDS scientists, right? You are a dimwit aren't you Paul, of course what I said applies, however it has nothing to do with HIV=AIDS or the validity of the clinical data that backs up that statement. It is simply a fact of life in this world and science seems to have dealt with it pretty effectively or we would still be bleeding folks and drilling holes in heads to release foul spirits which both make as much sense as claiming HIV is harmless.
Gary Stein
pauleewhiting - 04 Oct 2005 22:03 GMT "...of course what I said applies, however it has nothing to do with HIV=AIDS or the validity of the clinical data that backs up that statement."
Just like I said, Gary, "science has always been about money or power or both" with the one exception, of course, being the HIV theory of AIDS...
GMCarter - 05 Oct 2005 00:26 GMT >"...of course what I said applies, however it has nothing to do with >HIV=AIDS or the validity of the clinical data that backs up that >statement." > >Just like I said, Gary, "science has always been about money or power or >both" with the one exception, of course, being the HIV theory of AIDS... And also about discovery, health, hubris, arrogance--and all the various motivators of human beings.
So what?
This does NOT mean HIV does not exist or cause AIDS any more than cancer exists and causes disease. Or heart problems.
Does it have other consequences? You bet it does.
George M. Carter
pauleewhiting - 05 Oct 2005 02:24 GMT And also about discovery, health, hubris, arrogance--and all the various motivators of human beings.
So what?
This does NOT mean HIV does not exist or cause AIDS any more than cancer exists and causes disease. Or heart problems.
Does it have other consequences? You bet it does."
Yes, like people being given a terminal diagnosis based on non-specific anti-body tests, which are known to be highly cross-reactive.
And the results from those tests are then interpreted based on whether the patient belongs to a known "risk group."
That's why part of HIV testing includes a questionnaire to determine whether you fall into a known "risk group."
Thus, if you're Elisa and Western Blot tests come back positive and you're gay, you are determined to be HIV-positive based soley on the fact you are part of a "risk group" whose known "high-prevalencey of HIV infection" lends itself to your HIV diagnosis...
It's one of the finest examples of circular logic known to mankind.
wilyretrovirus - 05 Oct 2005 03:11 GMT Here's the formula.
You test "positive" on a non-specific antibody test because you're in a "high-risk group".
You're in a "high-risk group" because you test "positive" on a non-specific antibody test.
Where do I sign up?
BTW, George, I'm *still* waiting to meet my very first heterosexual caucasian male diagnosed "HIV-positive".
GMCarter - 05 Oct 2005 12:38 GMT snip
>Yes, like people being given a terminal diagnosis based on non-specific >anti-body tests, which are known to be highly cross-reactive. The Ab tests are very specific and NOT highly cross-reactive. See the other threads. This is an unsupported lie.
>And the results from those tests are then interpreted based on whether the >patient belongs to a known "risk group." As part of the overall diagnosis, yes.
>That's why part of HIV testing includes a questionnaire to determine >whether you fall into a known "risk group." [quoted text clipped - 3 lines] >part of a "risk group" whose known "high-prevalencey of HIV infection" >lends itself to your HIV diagnosis... I see. That's the answer you want and that works for you. Evidence to the contrary notwithstanding.
That's fine, dear. You go with that. You can believe whatever nonsense you like. So!
What's your creation myth look like? A big white guy with a beard dithering about in the dark til he lights a match? An infinite layer of turtles?
George M. Carter
pauleewhiting - 06 Oct 2005 04:48 GMT "And the results from those tests are then interpreted based on whether the patient belongs to a known 'risk group.'
As part of the overall diagnosis, yes."
pauleewhiting - 06 Oct 2005 04:52 GMT "This is an unsupported lie."
"Chemo does NOT cause CD4 cells to drop. They may cause other problems, like anemia. But that ain't a drop in CD4 count, etc."
"Chemotherapy can make you more likely to get infections. This happens because most anticancer drugs affect the bone marrow, making it harder to make white blood cells (WBCs), the cells that fight many types of infections."
Iconoclaster - 26 Sep 2005 00:57 GMT Paper #9: VA Study: HCV Increases Risk of Death Among HAART-Treated HIV+ Patients by 30-80%
More of the same.
Our analysis showed>" that HCV infection increases the risk of death in HIV patients who received HAART, controlling for numerous demographic and clinical factors, including exposure to HAART and response to HAART. Depending on the factors for which we controlled, we found that the risk of death among HAART-treated HIV patients was between 30% and 80% higher for those also infected with HCV."
With the same right, we could say that the risk of death is increased by HAART. We don't need 'HCV' in the equation. No evidence is presented, of course, that it exists. They just ASSUME it's there.
Iconoclaster - 26 Sep 2005 01:13 GMT Paper #10: Influence of Hepatitis C Virus Infection on HIV-1 Disease Progression and Response to Highly Active Antiretroviral Therapy"
This paper covers the same subject as paper #8. here is the main conclusion:
>" Conclusions. HCV serostatus did not affect the risk of HIV-1 disease progression, but the risk of liver disease-related deaths was markedly increased in HCV-seropositive patients. The overall virologic and immunologic responses to HAART were not affected by HCV serostatus."
Well now, that doesn't pull any punches, now does it? If you take HAART, you don't die of AIDS. You die of liver disease instead! Now doesn't that make you feel better?
Iconoclaster - 27 Sep 2005 01:46 GMT Paper #11: This paper aims at contradicting an earlier report (by other researchers) about stavudine and several other drugs causing steatosis.
>"We then focused on the use of stavudine in particular. Steatosis was observed in 53% of patients who had ever used stavudine (n = 51, mean grade 1.1, range 0-4), compared with the identical prevalence of steatosis (53%) in patients who had never used stavudine"
The reviewer, Jules Levin, notes: "Although study did not find difference between groups described above regarding incidence of steatosis, they did not look at patients separately who had glucose and lipid abnormalities, risk factors for steatosis. Although the differences below were not statistically significant, the number of patients in the study was small."
Actually, a fatty liver can have many causes. To list a few:
1. Obesity. 2. Alcohol. 3. Diabetes. 4. Medications like hormones, steroids, heart medications etc. 5. Several uncommon diseases of fat and carbohydrate metabolism. 6. Several diseases of the pancreas and intestines, all uncommon. 7. Malnutrition. 8. Other diseases.
"HCV" is taking a backseat here. It's a drug study.
Iconoclaster - 27 Sep 2005 02:01 GMT Paper #12: Promising Therapy for Human Hepatoma (liver cancer, HCC): Telomerase
I don't really have anything againt this paper, but... it deals with liver cancer chemotherapy:
>"Telomerase antagonists GRN163 and GRN163L inhibit tumor growth and increase chemosensitivity of human hepatoma"
Very interesting. But not a WORD about "HCV" (and rightfully so).
Iconoclaster - 27 Sep 2005 02:29 GMT Paper #13: Single (B or C), dual (BC or BD) and triple (BCD) viral hepatitis in HIV-infected patients in Madrid, Spain
>"Hepatitis was classified as follows: HB, positive serum HBsAg and negative serum HCV and HDV antibodies; HC, positive HCV antibodies and negative HBsAg; HBC, positive HBsAg, positive HCV antibodies and negative HDV total antibodies; HBD, positive HBsAg, positive total HDV antibodies and negative HCV antibodies; HBCD, positive HBsAg, positive HCV antibodies and positive total HDV antibodies."
Sí caballeros, those wily Spanyards have invented a Hep-D virus. Occurs only in Spain and Portugal, so far, but export to South-America is being considered. Obviously, there are data that cannot even be explained away with Hep-C, so they just came up with another one. You will notice from the quote above that all the tests are serological. They just say: These proteins are from HCV, and those are from HDV, and we're all supposed to believe that. I tend to believe in HBV, because I've actually seen evidence for the existence of Hep-B virus. But Hep-C, not to mention Hep-D... No evidence at all, and certainly not in this paper.
Iconoclaster - 27 Sep 2005 03:16 GMT Paper #15 Insulin resistance is a cause of steatosis and fibrosis progression in chronic hepatitis C
Did you ever play poker with your old-maid aunt? Lots of variants with Wild Cards. You can build any winning hand, using them. Well, HCV is such a Wild Card. You can invoke it any time you can't make heads or tails of the data:
>"The relationship between steatosis and fibrosis could be explained by several other mechanisms, such as lipid peroxidation.38-41 According to the "two hits hypothesis", steatosis could increase the sensitivity of hepatocytes to oxidative stress, the second hit being HCV infection itself in patients with chronic hepatitis C.39 Production of reactive oxygen species in an in vitro model expressing HCV core protein is consistent with this hypothesis."
Right. They just point a finger at a protein and say: "Tis is HCV core protein." But, just as in the case of 'HIV', there is no virus particle to check it against.
We're halfway through the 29 papers now, Mr. Stein. If the other half is just like the first half, I'll be seriously pissed.
robinhvd - 27 Sep 2005 06:46 GMT Iconoclaster, how can they not be as pointless as the first half -- look at the dates!? Please let us know if you find at least references to the seminal publications announcing the existence of HCV -- i.e. the Gallo papers of HCV. Happy reading.
Iconoclaster - 29 Sep 2005 20:48 GMT Paper #16: Hepatocellular carcinoma in 40 HIV/HCV-coinfected versus 50 HCV-monoinfected patients.
Whoever thinks that Mr. Stein's 29 papers are all peer-reviewed journal articles, better think again. This paper was presented at the International AIDS Conference in Rio de Janeiro, this summer. And it's a scream!
>"Only 1 of 90 patients was female. HIV/HCV patients were younger than HCV patients, and they consumed less alcohol."
In other words: The "HCV patients were old enough to have screwed up their liver with alcohol" The younger ones were told they were also infected with HIV, so their livers were destroyed with HAART.
>"Time from initial HCV infection to HCC was 7.5 years shorter in HIV/HCV compared to HCV patients (26.4 yrs, n=30, vs 35.2 yrs, n=62)."
(HCC =Hepatic Cellular Carcinoma) So it takes much less time to cancerize you liver with HAART than with any other toxic substance (such as alcohol or Tylenol).
>"Conclusions: HIV/HCV-coinfected patients develop HCC at a younger age than HCV-monoinfected patients due to a shorter interval from HCV infection to HCC. In contrast to the European study, we did not find a difference in survival between HIV/HCV and HCV patients."
As I mentioned already, Treatment for HIV (although they don't mention it) leads to liver cancer sooner that anything else. Of course there is no difference in survival: You have only one liver. And when you screw it up, you've had it.
This paper had no less than 13 (!) authors. Now be honest: Are my explanations in straight, simple language not far superior over the contrived hoopla of these 13 'experts'?
Iconoclaster - 29 Sep 2005 21:48 GMT Paper #17: Caucasians Had Better HCV Viral Load Reductions Than African-Americans During First 3 Days & During Weeks 1-4 After Starting Peg/RBV
Here they measure the difference in 'viral kinetics' between white and black people. The viruses (HIV and HCV)are measured as Viral Load. Of course the existence of these viruses never comes into play. They just have 2 jars with RNA snippets. One says: "This be HCV", and the other: "We call this HIV". They use them for PCR, so they can measure 'Viral Load'. And this VL goes down whenth patients are treated with PEGLFN and that frightening stuff, Ribavirin. And guess what? The Caucasians get their VL down to nothing faster than the Afro-Americans. Ideas anyone?
Iconoclaster - 29 Sep 2005 21:55 GMT Paper #18: Hepatitis C infection is not associated with systemic HIV-associated non-Hodgkin's lymphoma: a cohort study
>"Conclusions: In this immunocompromised patient population, there was no association between HCV infection and an increased risk of lymphoma."
Ah! The good news is that there's no bad news. And the bad news is that that's all the good news there is.
>"ED NOTE from Jules Levin: this is an important question and so we need better designed studies to tease out the possibility that HCV & HIV may cause higher rates of NHL in certain HIV+ patient populations."
Yeah. Better studies. I'm all for that.
Iconoclaster - 29 Sep 2005 22:33 GMT Paper #19: PI & NNRTI Drug Levels in Coinfected Patients
>"The study authors found that In HCV/HIV coinfected patients in this study Cmin "did not change significantly' for lopinavir, but the authors said NNRTIs "were strongly overdosed" in coinfected patients suggesting the need for drug monitoring in this population."
The cart before the horse. Is there really nobody who thinks of the posibility that high doses of NNRTIs cause liver damage, so that they have to postulate a virus (HCV) to blame for the damage? In other words, if you're already 'infected' with HIV (accoding to folklore), you become automatically 'co-infected' with HCV.
Iconoclaster - 29 Sep 2005 22:49 GMT Paper #20: Pegasys/RBV Improves Histology in Non-Responders & Cirrhotics
This is nothing but a clinical drug trial on patients with a bum liver. Not a word about HCV (oh well, why should there be?). The main conclusion is that COPEGUS (= ribavirin, the poison from hell) is so good. I wonder who financed this study...
GMCarter - 30 Sep 2005 13:02 GMT >Paper #20: Pegasys/RBV Improves Histology in Non-Responders & Cirrhotics > >This is nothing but a clinical drug trial on patients with a bum liver. Bullshit. This is what I mean. This cannot be passed off as an "analysis."
It is merely you spewing an unfounded and unqualified opinion.
George M. Carter
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